Cancer-fighting adenoviral vectors are now clinically available for intratumoral injection. However, the translation of this approach to the systemic treatment of metastatic tumors requires solutions to multiple obstacles including broad viral tropism, liver sequestration, hepatic toxicity, low-level coxsackie and adenovirus receptor (CAR) expression in some tumor types, and host immunity. See Barry et al., 11 CURR. OPIN. MOL. THER. 411-20 (2009); and Waehler et al., 8 NAT. REV. GENET. 573-87 (2007). Some of these problems have been overcome by genetically targeting the therapeutic effect through tissue-specific promoters or oncolytic mechanisms. For example, the first tissue-specific lytic adenovirus was developed for the treatment of prostate cancer (PCa) by limiting viral replication to cells containing activated androgen receptor. Rodriguez et al., 57 CANCER RES. 2559-63 (1997). These prostate-selective lytic vectors have been evaluated in clinical trials both as direct tumor injected agents and as systemically administered virus for castration-resistant metastatic PCa. Lipoid et al., 3 CANCER THER. 267-84 (2005). Although the therapeutic effect was limited to prostatic cells, the efficacy as a systemic therapy was hampered by viral sequestration and clearance. This reflects the loss of more than 90% of intravenously administered adenovirus through liver sequestration. Shashkova et al., 17 MOL. THER. 2121-30 (2009). Next generation cancer gene therapy vectors seek to enhance efficacy through capsid modifications designed to limit viral clearance and/or improve tumor infection through alternative receptors.